Cited by 46Protease and Inhibitor MechanismsCell death mechanisms and regulationGlioma Diagnosis and Treatment

Non-apoptotic Fas signaling regulates invasiveness of glioma cells and modulates MMP-2 activity via NFκB-TIMP-2 pathway

Wisniewski, Pawel, Ellert-Miklaszewska, Aleksandra, Kwiatkowska, Aneta, Kaminska, Bozena·2010·Cellular Signalling

Abstract

Fas (CD95/APO-1) is a cell surface "death receptor" that mediates apoptosis upon engagement by its ligand, FasL. Paradoxically, Fas/FasL can also promote cell invasion among non-apoptotic cells; here, we show that Fas/FasL signaling can promote tumor invasion when apoptosis is compromised. We have developed a recombinant FasL Interfering Protein (FIP) to interfere with Fas signaling in C6 glioma cells expressing both Fas receptor and its ligand. FIP administration did not affect cell viability but impaired cell motility and invasiveness of glioma cells. Blockade of Fas signaling reduced MMP-2 activity in glioma cells, that was associated with down-regulation of MAPK signaling, and AP-1 and NFkappaB-driven transcription. FIP treatment did not affect mmp-2 and mt1-mmp expression but significantly attenuated timp-2 expression and TIMP-2 amount in the culture medium. Studies with pharmacological inhibitors of JNK/c-Jun (SP600125) and NFkappaB (BAY11-7082) signaling pathways demonstrated that timp-2 expression is regulated by NFkappaB transcription factor. Our findings show that non-apoptotic Fas signaling activated in the autocrine manner or through microenvironment derived factors can regulate invasiveness of glioma cells via modulation of MMP-2 activation, likely by controlling TIMP-2 expression.

Integrity signals

Registry

Crossref · 10.1016/j.cellsig.2009.09.016

Cites

52 of 52 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • GOF mut-p53 has been shown to abnormally regulate a multitude of genes that play critical roles in glioblastoma pathogenesis, including CD95/Fas/Apo1, PARP, PTEN, and more.

    “Furthermore, GOF mut-p53 has been shown to abnormally regulate a multitude of genes that play critical roles in GBM pathogenesis, but have not been analyzed in the context of GBM. This includes CD95/Fas/Apo1, PARP, PTEN, and more [63,94,95,96,97,98].”

    From The p53 Pathway in Glioblastoma (2018) · cites this paper as [96]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Wisniewski, P., Ellert-Miklaszewska, A., Kwiatkowska, A., & Kaminska, B.
Affiliations
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
Corresponding author
Kaminska, Bozena
Venue
Cellular Signalling
Publisher
Elsevier BV
Published
2010-02
Volume
22
Issue
2
Pages
212-220
ISSN
0898-6568 (ISSN-L)
OpenAlex
W1968797465
Cited by
46
References
52
Citations by year
2026: 3 · 2024: 2 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 7 · 2016: 1 · 2015: 4 · 2014: 6 · 2013: 3 · 2012: 4
FWCI
1.34
Type
journal article
Language
en
Open access
closed
Locations
  • Cellular Signalling (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Science and Higher Education (P-N/024/2006, NN301 3945)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
Keywords
Fas/FasL signaling, glioma invasion, MMP-2 activity, TIMP-2, NF-κB, MAPK signaling, AP-1, tumor cell motility, autocrine signaling, tumor microenvironment
MeSH terms
Animals, Brain Neoplasms, Glioma, Humans, Neoplasm Invasiveness, Signal Transduction, Down-Regulation, NF-kappa B, Apoptosis, fas Receptor, Tissue Inhibitor of Metalloproteinase-2, Matrix Metalloproteinase 2, Cell Line, Tumor, JNK Mitogen-Activated Protein Kinases, Rats, Upstream Stimulatory Factors, Fas Ligand Protein

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review